SARS-CoV-2 infects human cardiomyocytes promoted by inflammation and oxidative stress
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SARS-CoV-2 infects human cardiomyocytes promoted by inflammation and oxidative stress. / Tangos, Melina; Budde, Heidi; Kolijn, Detmar; Sieme, Marcel; Zhazykbayeva, Saltanat; Lódi, Mária; Herwig, Melissa; Gömöri, Kamilla; Hassoun, Roua; Robinson, Emma Louise; Meister, Toni Luise; Jaquet, Kornelia; Kovács, Árpád; Mustroph, Julian; Evert, Katja; Babel, Nina; Fagyas, Miklós; Lindner, Diana; Püschel, Klaus; Westermann, Dirk; Mannherz, Hans Georg; Paneni, Francesco; Pfaender, Stephanie; Tóth, Attila; Mügge, Andreas; Sossalla, Samuel; Hamdani, Nazha.
In: INT J CARDIOL, Vol. 362, 01.09.2022, p. 196-205.Research output: SCORING: Contribution to journal › SCORING: Journal article › Research › peer-review
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TY - JOUR
T1 - SARS-CoV-2 infects human cardiomyocytes promoted by inflammation and oxidative stress
AU - Tangos, Melina
AU - Budde, Heidi
AU - Kolijn, Detmar
AU - Sieme, Marcel
AU - Zhazykbayeva, Saltanat
AU - Lódi, Mária
AU - Herwig, Melissa
AU - Gömöri, Kamilla
AU - Hassoun, Roua
AU - Robinson, Emma Louise
AU - Meister, Toni Luise
AU - Jaquet, Kornelia
AU - Kovács, Árpád
AU - Mustroph, Julian
AU - Evert, Katja
AU - Babel, Nina
AU - Fagyas, Miklós
AU - Lindner, Diana
AU - Püschel, Klaus
AU - Westermann, Dirk
AU - Mannherz, Hans Georg
AU - Paneni, Francesco
AU - Pfaender, Stephanie
AU - Tóth, Attila
AU - Mügge, Andreas
AU - Sossalla, Samuel
AU - Hamdani, Nazha
N1 - Copyright © 2022 The Author(s). Published by Elsevier B.V. All rights reserved.
PY - 2022/9/1
Y1 - 2022/9/1
N2 - INTRODUCTION: The respiratory illness triggered by severe acute respiratory syndrome virus-2 (SARS-CoV-2) is often particularly serious or fatal amongst patients with pre-existing heart conditions. Although the mechanisms underlying SARS-CoV-2-related cardiac damage remain elusive, inflammation (i.e. 'cytokine storm') and oxidative stress are likely involved.METHODS AND RESULTS: Here we sought to determine: 1) if cardiomyocytes are targeted by SARS-CoV-2 and 2) how inflammation and oxidative stress promote the viral entry into cardiac cells. We analysed pro-inflammatory and oxidative stress and its impact on virus entry and virus-associated cardiac damage from SARS-CoV-2 infected patients and compared it to left ventricular myocardial tissues obtained from non-infected transplanted hearts either from end stage heart failure or non-failing hearts (donor group). We found that neuropilin-1 potentiates SARS-CoV-2 entry into human cardiomyocytes, a phenomenon driven by inflammatory and oxidant signals. These changes accounted for increased proteases activity and apoptotic markers thus leading to cell damage and apoptosis.CONCLUSION: This study provides new insights into the mechanisms of SARS-CoV-2 entry into the heart and defines promising targets for antiviral interventions for COVID-19 patients with pre-existing heart conditions or patients with co-morbidities.
AB - INTRODUCTION: The respiratory illness triggered by severe acute respiratory syndrome virus-2 (SARS-CoV-2) is often particularly serious or fatal amongst patients with pre-existing heart conditions. Although the mechanisms underlying SARS-CoV-2-related cardiac damage remain elusive, inflammation (i.e. 'cytokine storm') and oxidative stress are likely involved.METHODS AND RESULTS: Here we sought to determine: 1) if cardiomyocytes are targeted by SARS-CoV-2 and 2) how inflammation and oxidative stress promote the viral entry into cardiac cells. We analysed pro-inflammatory and oxidative stress and its impact on virus entry and virus-associated cardiac damage from SARS-CoV-2 infected patients and compared it to left ventricular myocardial tissues obtained from non-infected transplanted hearts either from end stage heart failure or non-failing hearts (donor group). We found that neuropilin-1 potentiates SARS-CoV-2 entry into human cardiomyocytes, a phenomenon driven by inflammatory and oxidant signals. These changes accounted for increased proteases activity and apoptotic markers thus leading to cell damage and apoptosis.CONCLUSION: This study provides new insights into the mechanisms of SARS-CoV-2 entry into the heart and defines promising targets for antiviral interventions for COVID-19 patients with pre-existing heart conditions or patients with co-morbidities.
KW - COVID-19
KW - Humans
KW - Inflammation
KW - Myocytes, Cardiac
KW - Oxidative Stress
KW - SARS-CoV-2
U2 - 10.1016/j.ijcard.2022.05.055
DO - 10.1016/j.ijcard.2022.05.055
M3 - SCORING: Journal article
C2 - 35643215
VL - 362
SP - 196
EP - 205
JO - INT J CARDIOL
JF - INT J CARDIOL
SN - 0167-5273
ER -